New Research Suggests Memory Loss in Alzheimer’s Patients May be Reversible

New research from a team at MIT indicates symptoms of Alzheimer’s disease (AD) affecting patient’s memories may be reversible. AD causes memory loss by setting up genetic “blockades” formed when the enzyme HCAC2 condenses the genes of the brain responsible for memory. Eventually, those genes become useless; unexpressed, the genes are unable to cause the formation of new memories or retrieval of existing ones.

Clearly, blocking HCAC2 in the brain is an obvious fix; however, it has to date been impossible, in that all prior attempts have negatively affected the internal organs which require other enzymes in the histone deacetylase (HDAC) family for normal function. Researchers at MIT have now found something they hope might be the answer: LED lights which they use to prevent HCAC2 alone from binding with Sp3, its genetic blockade formation partner in crime (and Alzheimer’s).

Image Credit: jarmoluk/Pixabay

This research was spurred by the 2007 discovery that blocking HDAC activity in mice reversed memory loss. Human cells contain around one dozen forms of HDAC, and the team found later that it is HDAC2 that causes the memory-linked gene blockade, and that HDAC2 levels are elevated in Alzheimer’s patients.

Finding The Right Match

The trick was determining a way to target HDAC2 specifically without affecting HDAC1 levels and hurting white blood cell production as a result. To do this, the team analyzed postmortem brain samples of both healthy people and those with Alzheimer’s disease, assessing gene expression data. They found that there were more than 2,000 genes at levels that nearly matched HDAC2 levels. They then needed to test the best candidates; doing this allowed them to isolate the Sp3 gene.

“This is exciting because for the first time we have found a specific mechanism by which HDAC2 regulates synaptic gene expression,” Director of MIT’s Picower Institute for Learning and study lead author Li-Huei Tsai explained to MIT News. “If we can remove the blockade by inhibiting HDAC2 activity or reducing HDAC2 levels, then we can restore expression of all these genes necessary for learning and memory.”